Ventilation tubes how to delay their extrution?

Introduction:

Ventilation tubes are inserted to cure recurrent / frequent bouts of acute otitis media / chronic otitis media with effusion. Grommet insertion is particularly useful to treat patients with chronic mucoid otitis media.

Delay in insertion of ventilation tubes in these patients can cause chronic otitis media / chronic mastoiditis in these patients. Ventilation tubes measuring about 1.1 mm are known to last for atleast a year before being extruded. In patients with prolonged eustachean tube dysfunction these tubes help in prevention of atelectasis. If tubes measuring 1.5 mm are used they could stay in situ for prolonged duration thereby allowing adequate time for the middle ear healing process.

Studies have demonstrated that proper placement of these ventilation tubes can be helpful in delaying the process of extrusion.

Ventilation tubes should not be inserted in the postero superior quadrant because of the impending risk of incus dislocation. Similary placement in the postero inferior quadrant is also discouraged because of the risk of damage to round window. In this location there is also the added risk of damaging a high jugular bulb which could be an anatomical variant.

Classically the antero inferior quadrant is perferred because of the proximity to eustachean tube. Insertion in this area has one important flip side, i.e. Early extrusion of the ventilation tube.

Insertion of ventilation tune i.e. In the antero superior quadrant adjacent ot the handle of malleus and half way between the umbo and short process of malleus will serve the purpose of ventilation of middle ear adequately. Ventilation tubes placed in this quadrant have been known to stay in place for more than a year serving the important ventilatory function of middle ear cavity.

Anatomy of anterior ethmoidal artery

Introduction:

Anatomical knowledge of anterior ethmoidal artery is vital during endoscopic sinus procedures if complications are to be minimized. During its course the anterior ethmoidal artery crosses three cavities (the orbit, ethmoidal labyrinth and anterior cranial fossa of skull). The anterior ethmoidal artery enters the olfactory fossa through the lateral lamella of cribriform plate along the anterior ethmoidal sulcus. The bone over the anterior ethmoidal sulus is very thin and is at risk during endoscopic surgery. The relationship of the anterior ethmoidal artery to the roof of the ethmoid is highly variable and is at risk during endoscopic sinus surgeries. Identification of this artery is important in identifying frontal sinus outflow tract and superior limits of skull base.


Areas supplied by anterior ethmoidal artery:

It supplies the anteror ethmoidal cells and the frontal sinus. As it courses along the olfactory fossa it gives rise to meningeal vessels. This artery also supplies the anterior third of nasal septum and lateral nasal wall.

Stamberger reported that anterior ethmoidal artery may be in direct contact with skull base. This is particularly true if the roof of the ethmoid sinus is low. In majority of cases he reported that a bony mesentry could connect the anterior ethmoidal artery to the skull base. He also reported that there could be a space of about 5 mm between the anterior ethmoidal artery and skull base.

According to Gotwal who extensively studied the course of anterior ethmoidal artery by viewing coronal CT scans of nose and sinuses found that the presence of a notch in the medial wall of orbit indicates the probable site of antrior ethmoidal foramen. He also suggested that the presence of focal funneling in the olfactory fossa could indicate the probable position of anterior ethmoidal artery.

Coronal CT showing a dimple in the medial wall of orbit indicating the probable position of anterior ethmoidal artery canal.

Coronal CT showing anterior ethmoidal artery coursing close to skull base

Coronal CT paranasal sinuses showing the probable location of anterior ethmoidal artery close to the roof of frontal sinus and skull base.

Coronal CT showing anterior ethmoidal canal during its course through the anterior ethmoidal cells

What is angioneurotic oedema? Classify it on pathological basis and outline the management of a case with angioneurotic oedema.

Introduction:



Angioneurotic oedema is associated with rapid swelling of dermis, subcutaneous tissue, mucosa and submucosal tissues. It should be differentiated from urticaria where oedema occurs in the upper dermis. The term angioneurotic oedema is a misnomer which was used with the belief that nervous system was involved in some way as a causative factor. It was first introduced by Quinke in 1882. It was in 1888 Osler came out with a complete description of hereditary angioneurotic oedema.

The progression of angioneurotic edema could be very rapid and could even be life threatening. Major danger is airway compromise.



Classification:



Angioneurotic oedema can be classified into



Hereditary



Acquired.



Acquired angioneurotic oedema:

This is commonly caused by allergy and is usually associated with allergic symptoms like urticaria. It can also occur as a side effect to certain drugs (ACE inhibitors).



Hereditary angioneurotic oedema:

As the name suggests it is hereditary and is inherited as autosomal dominant form. This type is known to exist in three forms distinguished according to the underlying gene involvement. The first and the second forms as caused by abnormalities / mutations of SERPING1 gene. These mutations can cause decrease in the circulating levels of C1-inhibitor protein (type I hereditary anginoneurotic oedema) or dysfunctional forms of the same protein (this is type II hereditary angioneurotic oedema). Type III hereditary angioneurotic oedema is associated with mutations of F12 gene. This gene is supposed to encode the coagulation factor 12. Almost all these forms of hereditary angioneurotic odema cause abnormal activation of complement system and cause swelling / oedema in other regions of the body like digestive tract. If this swelling involves larynx it can compromise the airway.



Signs / symptoms:



The following areas may become swollen within minutes to hours:



Skin of the face and around the mouth

Mucosa of mouth and throat

Tongue

Hands

Decreased sensation due to compression of nerves

Airway compromise / stridor

In acquired angioneurotic oedema exposure history of allergen can be elicited



In hereditary angioneurotic oedema there is not obvious cause. It could be as trivial as mild trauma / dental scaling etc. These patients do not exhibit urticaria / allergic rashes as it is not an allergic response. These patients may manifest with acute abdominal pain and watery diarrhoea. Acute abdominal pain is also associated with lymphocytosis. Swelling may also occur in the extremities.



Investigations:



Complete blood count

Renal function tests

Serum electrolyte estimation ( in cases of diarrhoea)

Mast cell tryptase levels may be raised in acquired angioneurotic oedema

Deficiency of C1 inhibitor

Depletion of complement factors 2 and 4 indicate deficiency of C1 inhibitor



Hereditary angioneurotic oedema can be identified when the patient fails to respond to antihistamines and steroids.



Pathophysiology:



Bradykinin plays a vital role in the pathogenesis of all forms of angioneurotic oedema. This peptide is a potent vasodilator which increases vascular permeability causing rapid accumuation of fluid in the interstitium. Reducing / blocking this peptide plays a vital role in alleviating the symptoms.

ACE inhibitors block ACE the enzyme that is responsible for deactivation of bradykinin. It should be borne in mind that bradykinin is produced by continuous activation of complement system. Complement system is continuosly activated by deficiency of C1 esterase which is a potent inhibitor of complement system. This is made possible due to continuous production of Kallikrein.



Differences between the three types of hereditary angioneurotic odemea:



Type I : Decreased levels of C1 inhibitor



Type II : Normal levels of C1 inhibitor but decreased function



Type III : There is no abnormality involving C1 inhibitor, and is an X linked dominant disorder mainly affecting females. This condition can be exacerbated by pregnancy / contraceptive pills and other hormone therapy.



Aggravating factors:



Consumption of food that causes vasodilatation (alcohol / cinnamon)

Use of Ibuprofen / aspirin may increase the probablity in some patients



Use of Bromelain in combination with turmeric has been proved to be beneficial in certain cases.



Management:



Allergic – In allergy induced angioneurotic oedema avoidance of allergen and use of antihistamines may prevent future attacks. Cetrizine is the commonly prescribed antihistamine in the management of allergic angioneurotic oedema. Severe allergic angioneurotic oedema may require desensitization if the putative allergen could be identified. Use of steroids have also found to be beneficial in these patients.









Drug induced angioneurotic oedema: Common drugs involved include ACE inhibitor. Avoidance of these drugs will help.



Hereditary angioneurotic oedema : Since C1 Inhibitor is deficient in these patients C1 inhibitor concentrates can be administered. In acute cases frozen plasma may be beneficial as it contains adequate amounts of C1 inhibitor.

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Histological classification of fungal sinusitis

Four distinct histologic categories of fungal sinusisits have been recognised. This classification goes a long way in deciding the optimal management modality in patients suffering from this condition.

1. Allergic fungal sinusitis
2. Non invasive fungal colonization (fungal ball)
3. Chronic invasive fungal sinusitis
4. Acute fulminant fungal sinusitis

Acute fulminant fungal sinusitis is commonly seen in immunocompromised / diabetic patients. This can really be fatal and hence need to be treated aggressively with systemic antifungal agents.

Allergic fungal sinusitis does not require antifungal therapy but should be treated aggressively for the underlying allergy. Aim of treating these patients aggressively is to reduce the incidence of recurrence rates. After surgical removal of the disease these patients should be treated with corticosteroids with simultaneous montoring of serum IgE levels. This also reduces clinical symptoms. Current management modalities also include antileukotriene agents.

Allergic fungal sinusitis can be suspected if allergic mucin is present in the specimen. This mucin is a special type and could be green, brown or black in color. The material present has a consistency of that of clay and the cut surface appears laminated. Microscopically allergic mucin appears eosinophilic on H&E stain. There is also associated presence of charcot leyden crystals and eosinophils. The mucosal tissue demonstrated changes consistent with that of inflammatory polyposis.

Histological diagnosis of non invasive fungal sinusitis is really easy as fungal organims can be clearly seen in abundance under H&E.

Acute fulminant sinusitis is characterised by tissue invasion by fungal organism. In this type angioinvasion is really common in contrast chronic invasive fungal sinusitis is characterised by tissue invasion and formation of granulation tissue.

Currently one more entity has been added.

EMRS: (eosinophilic mucin rhinosinusitis)

This entity is characterised by the presence of allergic mucin but fungal hyphae is not evident. Fungal cultures too turn out to be negative.

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Vestibular system evaluation in paediatric patients

Introduction:

Early identification of auditory disorders in infants and children are common these days. Similarly now the focus is shifting on early diagnosis of vestibular system disorders in children. Earlier identification of audio vestibulo disorders in children leads to the development of early remedial stratergies. A reliable and complete history is must in order to accurately diagnose diseases of vestibular system. The challenges that confront the otolaryngologist in evaluating patients of pediatric age group are the inability of the patient to describe the symptoms in detail and the prohibitive cost of the equipments used to examine the vestibular system of these patients.

Physical examination:
No equipment could replace a good physical examination. As a first step it imperative on the part of the examiner to win the confidence of the patient. Unless a child co operates physical examination is virtually impossible.

Looking for the presence / absence of spontaneous / gaze evoked nystagmus should be the preliminary step. If the child is able to follow simple verbal commands it can be asked to look straight ahead (spontaneous nystagmus will become evident now). The child may be asked to follow the fingers of the examiner in both horizontal and vertical directions. Gaze evoked nystagmus if present will become evident.

Dynamic evaluation:
In this evaluation consideration should be given to testing “Head shake nystagmus”. This is also known as vestibuloocular reflex. This reflex is readily observed by the age of 9-12 months in normal developing infants. Movement of the eyes can be better appreciated by using Frenzel glasses / electro oculography / infra red video. In this test the child's head is gently rotated back and forth in a rhythmic horizontal manner. Nystagmus will be observed only in children with vestibular asymmetry. Head shake nystagmus evaluation will help in those situations when it is not feasible to perform bithermal caloric test or rotatory chair testing. Under normal circumstances while performing this test the eyes of the child will move smoothly on either side. Any catch up saccades of nystagmus will point towards the diagnosis of vestibular dysfunction.

Dynamic visual acuity techniques:
This test is actually a modification of Snellen's eye chart. In this test a baseline is obtained by discerning the distance from which the child can discern the smallest line of characters from a fixed distance. While the child is attempting to read the smallest line the head is rotated back and forth with the approximate frequency of 1-2 Hz. While reading loss of one line may be considered insignificant while loss of three lines should be considered to be significant. This indicates VOR deficiency.

Positional testing:

BPPV is rather rare in children. They may rarely experience positional vertigo which can be testing by putting the child in the provoking position. Before performing positional tests like Dix Hall Pike maneuver it is of paramount importance to win the trust of the child. The examiner assists the patient in turning the head to the right or left when the child is lying on its back. The eye is observed for the presence or absence of nystagmus.



Tests for cerebellar functions:

This can be easily assessed in a child by asking it to perform marching on the spot test/ tandem walking test etc.

Video oculography:
The equipment used has an infrared video camera mounted in eye goggles. This effectively replaces electrodes used to record eye movements. This procedure includes a battery of tests which are used to discern peripheral and central nystagmus.
The test battery include:
Looking for spontaneous nystagmus
Looking for gaze nystagmus
Measuring positioning and positional nystagmus
Perfroming bithermal caloric irrigations
It should be borne in mind that the child should stop taking drugs for cough and cold two days prior to testing. The child should have eaten only lightly before the test. Video oculography is usually performed in a darkened room in order to avoid eye fixation. Children will be comfortable in dark only in the presence of their parents. Illuminated cartoon characters can be used to maximize the attention of the children.

Computerized rotatory chair:
This test complements the vestibular evaluation battery of tests. This test helps when other vestibular function tests are inconclusive. Since multiple frequencies are used in this test the accuracy is much more. The computerized rotatory chair for paediatric use has some slight modifications. This test uses sinusoidal harmonic acceleration its accuracy is enhanced. The whole enclosure is darkened and is designed in such a way that it resembles a space ship. The enclosure should be fairly big enough to accomodate the parent and the child who should sit on their lap. It should also be provided with a talk back system through which the examiner must be constantly communicating with the child. The following parameters of the test are considered for evaluation:

Gain
Phase
Symmetry

Gain is a measure that refers to the strength of the reflex and is calculated by dividing slow phase eye velocity by that of chair velocity (This is an indirect reference to head velocity). Children usually demonstrated higher gain values than adults at frequencies of 0.08 and 0.5Hz.

Phase refers to the timing of the response i.e eye movement in comparison with that of head turning movement. When the phase is less than zero, the eye velocity lags behind head velocity and when the phase value is greater than zero then the eye velocity leads the head velocity.
Symmetry helps in identifying unilateral vestibular disorders.
Step velocity test using computerized rotatory chair can be performed in preschool children and adolescents. The patient seated in the rotatory chair is rotated in one direction at approximately 100 degrees / second. The build up of nystagmus activity as the rotating chair accelerates is recorded. When a steady state of rotation is reached then nystagmus begins to fade. The per rotatory nystagmus beats in the same direction as the rotation (right beating nystagmus during clockwise rotation). The vestibular time constant is measured for each rotation. Vestibular time constant is defined as the amount of time necessary for the per rotatory nystagmus to diminish to 37% of its original intensity. On sudden stopping of the chair post rotatory nystagmus would return. It should also be measured in terms of vestibular time constant.


Computerized rotatory chair enclosures can be used to perform optokinetic testing.

Visual vestibular interactions: This is another test which could be performed using computerized rotatory chair. Patient views strips projected on the enclosure wall as the chair rotates. The resultant nystagmus is recorded using a tracking device.

Computerized dynamic posturography:

It helps in assessing the balance as a function. It breaks down the relative contributions of visual, proprioceptive and vestibular clues. The patient is made to stand on a platform wearing safety harnesses and is made to face a visual surround. The platform contains sensors that measure the force exerted by the feet when the centre of gravity changes. The most commonly performed test using this equipment is Sensory organization test. In this test the patient is supposed to maintain the best balance possible despite conflicting visual and proprioceptive clues.
Motor control test is another test that is performed with this equipment. In this test the platform experiences unexpected peturbations which are classified as small, medium and severe in degrees. These peturbations take place in both forward and backward directions. The patients ability to maintain balance even during these perturbations is used as an index.

Adaptation test: This is another test that can be performed with this equipment. In this test the platform moves unexpectedly upwards / downwards in such a way that the toe either points upwards or downwards. The patient's ability to regain balance is measured.

The child should be rewarded on completion of each test as this would motivate the child to take the entire battery of tests.

VEMP:

This stands for vestibular evoked myogenic potentials. This test is rather quick to perform and easy to interpret. The purpose of this test is to determine if the saccule, portions of otoliths, inferior vestibular nerve and its central connections are intact and working normally. The saccule which is the lower otolith organ has mild sensitivity to sound. This sensitivity can actually be measured and is considered to be a remnant of its evolutionary function. The vemp recording is usually made from an electrode placed at the level of sternomastoid muscle.

VEMP pathway:
Sound stimulates the saccule
It activates the inferior vestibular nerve
Lateral vestibular nucleus is activated next
11th nerve nucleus and ipsilateral sternomastoid muscle is stimualted.

Conductive hearing losses obliterate vemp while sensorineural hearing loss doesn't affect it.

Sound stimulus is delivered as loud clicks / tone bursts atleast 90 – 100dB sound pressure level. Sound is usually presented at 200 ms intervals. Optimum frequency is between 500 – 1000 Hz. The sternum is usually used for reference electrode and the forehead for reference electrode.